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Endogenous molecular circadian clocks drive daily rhythmic changes at the cellular, physiological, and behavioral level for adaptation to and anticipation of environmental signals. The core molecular system consists of autoregulatory feedback loops, where clock proteins inhibit their own transcription. A complex and not fully understood interplay of regulatory proteins influences activity, localization and stability of clock proteins to set the pace of the clock. This study focuses on the molecular function of Ribosomal S6 Kinase (RSK) in the Drosophila melanogaster circadian clock. Mutations in the human rsk2 gene cause Coffin–Lowry syndrome, which is associated with severe mental disabilities. Knock-out studies with Drosophila ortholog rsk uncovered functions in synaptic processes, axonal transport and adult behavior including associative learning and circadian activity. However, the molecular targets of RSK remain elusive. Our experiments provide evidence that RSK acts in the key pace maker neurons as a negative regulator of Shaggy (SGG) kinase activity, which in turn determines timely nuclear entry of the clock proteins Period and Timeless to close the negative feedback loop. Phosphorylation of serine 9 in SGG is mediated by the C-terminal kinase domain of RSK, which is in agreement with previous genetic studies of RSK in the circadian clock but argues against the prevailing view that only the N-terminal kinase domain of RSK proteins carries the effector function. Our data provide a mechanistic explanation how RSK influences the molecular clock and imply SGG S9 phosphorylation by RSK and other kinases as a convergence point for diverse cellular and external stimuli.
Honest actions predominate human behavior. From time to time, this general preference must yield to dishonest actions, which require an effortful process of overcoming initial honest response activation. This thesis presents three experimental series to elucidate this tug-of-war between honest and dishonest response tendencies in overtly committed instances of lies, thereby joining recent efforts to move from a sheer phenomenological perspective on dishonest responding as being more difficult than honest responding to a precise description of the underlying cognitive processes. The consideration of cognitive theories, empirical evidence, and paradigms from different research fields – dishonesty, cognitive control and sensorimotor stage models of information processing – lay the groundwork for the research questions and methodological approach of this thesis.
The experiments pinpoint the underlying conflict of dishonest responding in the central, capacity-limited stage of information processing (Experiments 1 to 4), but they also demonstrate that cognitive control processes (Experiments 5 to 7) and the internalization of false alibis (Experiments 8 to 11) can reduce or even completely eliminate this conflict. The data reveals great flexibility at the cognitive basis of dishonest responding: On the one hand, dishonest responding appears to rely heavily on capacity-limited processes of response selection to overcome honest response tendencies alongside up- and downstream consequences of response activation and monitoring. On the other hand, agents have powerful tools to mitigate these effortful processes through control adaptation and false alibis. These results support and expand current theorizing of the cognitive underpinnings of dishonest responding. Furthermore, they are alerting from an applied perspective on the detection of lies, especially when considering the flexibility of even basic cognitive processes in the face of false alibis. A promising way to move forward from here would be a fine-grained discrimination of response activation, passive decay and active inhibition of honest representations in dishonest responding and the assessment of the adaptiveness of these processes.